Rubio-Reynoso R , Chávez-Iñiguez JS , López-Iñiguez A , Valerdi-Contreras L , Martin-Nares E , Ontiveros-Mercado H , Castro-Gallegos E

Language: Spanish
References: 12
Page: 161-165
PDF size: 806.50 Kb.

ABSTRACT

In the acute kidney damage the urinary sediment helps to discriminate the damage between pre-renal and acute tubular necrosis. No predictor index of acute tubular necrosis based on urinary sediment takes into account the alterations in the morphology of the erythrocyte. The erythrocyte dysmorphism in acute tubular necrosis is not frequent. We present the case of a 31 years old male who attends because of abdominal pain and vomiting. In his background, alcoholism and smoking. Denies chronic diseases. After the examination, arterial blood pressure of 85/40 mmHg, heart rate of 116. He was dehydrated, with Kussmaul breathing and basal crepitant rales with diminished peristalsis, generalized abdominal pain. With the following diagnoses: diabetic ketoacidosis, community-acquired pneumonia and pancreatitis. The patient is treated with rehydration, IV insulin and antibiotics. Blood glucose levels normalize but the patient continued with metabolic acidosis and began a respiratory deterioration requiring mechanical ventilation. In spite of the reanimation, the creatinine increased, presenting oliguria, acidemia and hyperkalemia. He is treated with hemodialysis, solving the metabolic acidosis. The creatinine continues increasing. The urinary sediment presents erythrocyte dysmorphism in more than 95%. Raising the suspicion of glomerular hematuria but the immunological approach reports negative. A kidney biopsy reports acute tuburlar necrosis, without glomerular alterations. After 8 days of admission and 4 sessions of hemodialysis, the creatinine is reported in 1.02g/dl. After 30 days the patient shows normal levels of creatinine.

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